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正常受试者存在胰岛素-肾素-醛固酮-钾的相互关系,而在慢性血液透析患者中这种关系被破坏。

Presence of insulin-renin-aldosterone-potassium interrelationship in normal subjects, disrupted in chronic hemodialysis patients.

作者信息

Farfel Z, Iaina A, Eliahou H E

出版信息

J Clin Endocrinol Metab. 1978 Jul;47(1):9-17. doi: 10.1210/jcem-47-1-9.

DOI:10.1210/jcem-47-1-9
PMID:400716
Abstract

The factors regulating aldosterone secretion in normals and in patients on chronic hemodialysis were studied by the determination of the circadian rhythm of plasma aldosterone, renin, cortisol, insulin, potassium, sodium, and glucose. Four normal volunteers and eight normotensive patients on regular dialysis treatment (RDT) were studied during prolonged recumbency on low sodium diet. A definite circadian rhythm for renin could not be demonstrated in RDT patients. The significant simple and multiple correlation coefficients found in normal subjects suggest that insulin participates in the regulation of aldosterone together with the other known factors: ACTH, renin, and potassium. In chronic renal failure, however, when basal conditions were maintained during prolonged recumbency, the correlations of insulin and renin with aldosterone were not found, suggesting that in this condition aldosterone secretion is controlled by ACTH and potassium. As a direct influence of insulin on aldosterone could not be demonstrated by multiple variance analysis, it seems that insulin is related to aldosterone indirectly through renin and/or potassium. The presence of significant correlations between insulin-potassium and potassium-aldosterone in RDT patients, without a significant insulin-aldosterone correlation, suggest that in the normals insulin participates in aldosterone regulation through renin secretion and not through potassium. A correlation between potassium and renin was not found in normals or in RDT patients.

摘要

通过测定血浆醛固酮、肾素、皮质醇、胰岛素、钾、钠和葡萄糖的昼夜节律,研究了正常人和慢性血液透析患者中调节醛固酮分泌的因素。对4名正常志愿者和8名接受常规透析治疗(RDT)的血压正常患者在低钠饮食下长时间卧床期间进行了研究。在接受RDT治疗的患者中未发现肾素存在明确的昼夜节律。在正常受试者中发现的显著单因素和多因素相关系数表明,胰岛素与其他已知因素(促肾上腺皮质激素、肾素和钾)一起参与醛固酮的调节。然而,在慢性肾衰竭中,当长时间卧床期间维持基础状态时,未发现胰岛素和肾素与醛固酮之间存在相关性,这表明在这种情况下醛固酮分泌受促肾上腺皮质激素和钾的控制。由于多因素方差分析未显示胰岛素对醛固酮有直接影响,似乎胰岛素通过肾素和/或钾间接与醛固酮相关。在接受RDT治疗的患者中,胰岛素与钾、钾与醛固酮之间存在显著相关性,但胰岛素与醛固酮之间无显著相关性,这表明在正常人中胰岛素通过肾素分泌而非钾参与醛固酮调节。在正常人和接受RDT治疗的患者中均未发现钾与肾素之间存在相关性。

相似文献

1
Presence of insulin-renin-aldosterone-potassium interrelationship in normal subjects, disrupted in chronic hemodialysis patients.正常受试者存在胰岛素-肾素-醛固酮-钾的相互关系,而在慢性血液透析患者中这种关系被破坏。
J Clin Endocrinol Metab. 1978 Jul;47(1):9-17. doi: 10.1210/jcem-47-1-9.
2
Control of plasma aldosterone during hemodialysis in patients with terminal renal failure.终末期肾衰竭患者血液透析期间血浆醛固酮的控制
Nephron. 1977;18(2):114-23. doi: 10.1159/000180785.
3
[The regulation of plasma aldosterone in hemodialysis patients].[血液透析患者血浆醛固酮的调节]
Schweiz Med Wochenschr. 1980 Dec 6;110(49):1882-4.
4
Circadian rhythm and effect of posture on plasma aldosterone concentration in primary aldosteronism.原发性醛固酮增多症中昼夜节律及体位对血浆醛固酮浓度的影响
J Clin Endocrinol Metab. 1976 Jul;43(1):115-31. doi: 10.1210/jcem-43-1-115.
5
The effect of spironolactone in hypertensive patients on regular haemodialysis and after renal allotransplantation.螺内酯对接受定期血液透析和肾移植后的高血压患者的影响。
Life Support Syst. 1983 Jul-Sep;1(3):197-205.
6
Effect of various therapeutic approaches on plasma potassium and major regulating factors in terminal renal failure.各种治疗方法对终末期肾衰竭患者血钾及主要调节因子的影响
Am J Med. 1988 Oct;85(4):507-12. doi: 10.1016/s0002-9343(88)80086-x.
7
Aldosterone response to insulin-induced hypoglycemia in hemodialysis patients.血液透析患者对胰岛素诱导的低血糖的醛固酮反应。
Am J Nephrol. 1989;9(3):215-21. doi: 10.1159/000167968.
8
Control of plasma aldosterone in terminal renal failure before and after nephrectomy and after renal transplantation.
Clin Nephrol. 1976 Oct;6(4):433-6.
9
The effect of dexamethasone on the control of plasma aldosterone concentration in normal recumbent man.地塞米松对正常卧位男性血浆醛固酮浓度控制的影响。
J Lab Clin Med. 1975 Jun;85(6):957-67.
10
Response of plasma aldosterone to sequential ultrafiltration, dialysis and conventional hemodialysis.
Nephron. 1980;26(6):274-9. doi: 10.1159/000182001.

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